This invention relates to the feeding of non-protein nitrogen (NPN) compounds, such as urea and the like, to ruminants. More particularly, it concerns improvements which permit the use of larger amounts of NPN compounds without encountering toxicity and related difficulties.
All animals require protein. Simple-stomached animals such as swine and poultry require preformed protein, for vegetable or animal sources, in their diets, but ruminant animals are uniquely different. Microorganisms found in the rumens (paunch, or first stomach) of cattle, sheep, goats, and other ruminants allow the animal to manufacture protein amino acid from simple nitrogen compounds. Apparently, non-protein nitrogen (NPN) compounds such as urea or biuret are first converted to ammonia through the action of urease or biurease enzyme produced by the rumen microorganisms, which then utilize the ammonia to synthesize protein amino acids which can be digested by the ruminants digestive system.
This ability of ruminants to utilize NPN compounds as indirect protein sources has important economic consequences for the farmer. By substituting NPN compounds for a portion of the natural protein, major economies are realized. See the book "Urea as a Protein Supplement" by M. M. Briggs (Pergamon, 1967).
One pound of urea is equivalent in nitrogen content to over five pounds of a high protein feed such as soy bean oil meal. On the basis of relative cost per unit of nitrogen, in 1970 soy bean oil meal cost over seven times as much as urea; in early 1973, the relative cost ratio increased to over twelve to one. As a consequence, there is a strong incentive to replace a portion, or even all, of the vegetable protein fed to ruminants with NPN compounds.
Unfortunately the amount of NPN compound that a ruminant can ingest is quite limited. The ammonia, or its equivalent ammonium ion, produced during post-feeding fermentation when the NPN compound is decomposed can be transferred to the blood stream across the rumen wall. When high levels of blood ammonia occur, the acid-base balance of the blood changes, and the central nervous system is affected. Early toxic symptoms are bloat, incoordination, labored breathing, and excessive salivation; in extreme cases there may be convulsions and death.
Various attempts have been made to limit the ammonia concentration in the rumen so as to permit the use of more NPN compound in the daily ration. Antiurease compounds, somewhat more stable urea derivatives, coated urea particles, replacement of urea with biuret, and homogeneous admixture of the NPN compound with all of the feed, have been proposed. All have had qualified success.